Background The impact of an adverse prenatal environment such as famine exposure on the development of adulthood non-communicable chronic illnesses, including diabetes and hypertension has been well articulated in the recent past and supported by evidence. However, there exist few longitudinal studies conducted on the long term consequences of prenatal famine exposure on adulthood kidney function. Hence, we set out to examine whether prenatal exposure to the Ethiopian Great Famine (1983–1985) was associated with changes in estimated glomerular filtration rate (eGFR) and the risk of developing chronic kidney disease (CKD) later in adult life. Methods The study was conducted in 219 famine exposed and 222 non exposed cohorts in Raya Kobo district, North Wollo Zone, Northern Ethiopia. Estimated GFR was computed from standardized serum creatinine using the CKD Epidemiology Collaboration (CKD-EPI) equation. The definition of CKD includes those with an eGFR of less than 60 ml/min/1.73 m2 on at least in two occasions of 90 days apart (with or without markers of kidney damage). Linear and logistic regression analyses were employed to examine the independent effect of prenatal famine exposure on eGFR and CKD respectively. Results The mean (SD) serum creatinine of exposed and non-exposed groups were 0.78 (0.2) and 0.75 (0.2) respectively. The mean (SD) eGFR of exposed groups was 107.95 (27.49) while the non-exposed 114.48 (24.81) ml/min. In linear regression, the unadjusted model to examine the association between famine exposure and eGFR resulted in a significant negative beta coefficient (β = − 0.124: 95% CI: − 11.43, − 1.64). Adjusting the exposure for outstanding covariates of kidney health, including systolic blood pressure, fasting blood sugar and blood glucose did not alter the inverse relationship (β = −.114 95% CI: − 10.84, − 1.17). In the unadjusted bivariate logistic regression model, famine exposure resulted in nearly 2.7 times higher odds of developing CKD (OR: 2.68, 95% CI: 1.16, 6.2). The odds remained equivalent after adjusting for systolic blood pressure, fasting blood glucose and body mass index (OR = 2.61: 95% CI: 1.120, 6.09). Conclusion In the study setting, prenatal exposure to the Great Ethiopian Famine was associated with decreased eGFR and higher risk of developing CKD among survivors. These findings may imply that famine in early life may play a significant role in the development of kidney dysfunction in adulthood.

Background: The impact of an adverse prenatal environment such as famine exposure on development of adulthood non communicable chronic illnesses, including diabetes and hypertension has been well articulated in the recent past and supported by evidence. However, there exist a limited number of longitudinal studies on long term consequences of prenatal famine on adulthood kidney function. Hence, we set out to examine whether prenatal exposure to the Ethiopian Great Famine (1983–1985) was associated with changes in estimated glomerular filtration rate (GFR) and risk of developing chronic kidney disease (CKD) during adulthood.Methods: The study was conducted in 219 famine exposed and 222 non exposed cohorts in Raya Kobo district, North Wollo Zone, Northern Ethiopia. Estimated GFR was computed using the CKD Epidemiology Collaboration (The CKD-EPI) equation. CKD was defined as eGFR= <60 mL/min per 1.73 m2. Linear and logistic regression analyses were employed to examine the independent effect of prenatal famine exposure on eGFR and CKD respectively.Results: The mean (SD) serum creatinine of exposed and non-exposed groups were 0.78 (0.2) and 0.75 (0.2) respectively. The mean (SD) eGFR of exposed groups was 107.95 (27.49) while the non-exposed 114.48 (24.81) ml/min. In linear regression, unadjusted model to examine the association between famine exposure and eGFR resulted in a significant negative beta coefficient (β = -0.124: 95% CI: -11.43, -1.64). Adjusting the exposure for outstanding covariates of kidney health, including systolic blood pressure, fasting blood sugar and blood glucose did not alter the inverse relationship (β = -.114 95% CI:-10.84, -1.17). In binary unadjusted logit model, famine exposure resulted in nearly 2.7 times increased odds of developing CKD (OR: 2.68, 95% CI: 1.16, 6.2). The odds remained equivalent after adjusting for systolic blood pressure, fasting blood glucose and BMI (OR= 2.61: 95% CI: 1.120, 6.09).Conclusion: prenatal exposure to the Great Ethiopian Famine was associated with decreased eGFR and greater risk of CKD among survivors. These findings may imply that famine in early life may play significant role in the development of kidney dysfunction in adulthood.

Background: The impact of an adverse prenatal environment such as famine exposure on the development of adulthood non-communicable chronic illnesses, including diabetes and hypertension has been well articulated in the recent past and supported by evidence. However, there exist few longitudinal studies conducted on the long term consequences of prenatal famine exposure on adulthood kidney function. Hence, we set out to examine whether prenatal exposure to the Ethiopian Great Famine (1983–1985) was associated with changes in estimated glomerular filtration rate (eGFR) and the risk of developing chronic kidney disease (CKD) later in adult life.Methods: The study was conducted in 219 famine exposed and 222 non exposed cohorts in Raya Kobo district, North Wollo Zone, Northern Ethiopia. Estimated GFR was computed from standardized serum creatinine using the CKD Epidemiology Collaboration (CKD-EPI) equation. The definition of CKD includes those with an eGFR of less than 60 ml/min/1.73m2 on at least in two occasions of ninety days apart (with or without markers of kidney damage). Linear and logistic regression analyses were employed to examine the independent effect of prenatal famine exposure on eGFR and CKD respectively.Results: The mean (SD) serum creatinine of exposed and non-exposed groups were 0.78 (0.2) and 0.75 (0.2) respectively. The mean (SD) eGFR of exposed groups was 107.95 (27.49) while the non-exposed 114.48 (24.81) ml/min. In linear regression, the unadjusted model to examine the association between famine exposure and eGFR resulted in a significant negative beta coefficient (β = -0.124: 95% CI: -11.43, -1.64). Adjusting the exposure for outstanding covariates of kidney health, including systolic blood pressure, fasting blood sugar and blood glucose did not alter the inverse relationship (β = -.114 95% CI: -10.84, -1.17). In the unadjusted bivariate logistic regression model, famine exposure resulted in nearly 2.7 times higher odds of developing CKD (OR: 2.68, 95% CI: 1.16, 6.2). The odds remained equivalent after adjusting for systolic blood pressure, fasting blood glucose and body mass index (OR= 2.61: 95% CI: 1.120, 6.09).Conclusion: In the study setting, prenatal exposure to the Great Ethiopian Famine was associated with decreased eGFR and higher risk of developing CKD among survivors. These findings may imply that famine in early life may play a significant role in the development of kidney dysfunction in adulthood.

Background Previous famine studies reported the inverse link between early life nutritional deprivation and adulthood optimal health outcomes. However, there remain sparse data on the impact of early life famine exposure in later life economic achievement. Hence, we set out to examine the association of early life famine exposure on economic achievement among survivors of the 1983–85 great Ethiopian famine. Method A historical cohort study design was employed among 968 adult men and women in the Raya Kobo district, Northern Ethiopia. Participants were categorized into in utero exposed, postnatal exposed and unexposed groups based on self-reported age and birthdate. Structured questionnaire was used to collect data on socio-demographic and individual assets. Principal component analysis (PCA) was used to determine wealth index as proxy for economic achievement. Multinomial logistic regression analyses were employed to examine the independent effect of early life famine exposure on the outcome. Results In unadjusted model, compared to unexposed cohorts, in utero and postnatal famine exposed cohorts were nearly twice more likely to fall in the lowest wealth category (OR: 1.93, 95% CI: 1.40, 2.64) and (OR: 2.12, 95%CI: 1.45, 3.08), respectively. However, these associations became non-significant when adjusted for biologic and demographic variables (P > 0.05). Instead, educational status appeared to have significant association with wealth; those who can’t read or write among in utero and postnatal exposed group were three times more likely to fall in low wealth index category than those who achieved secondary and above level of education (OR = 3.00 95% CI: 1.74, 5.18) and (OR = 2.92, 95% CI: 1.48, 5.76), respectively. Similarly, those with primary education among in uero and postnatal famine exposed cohorts were twice more likely to fall in the low wealth index than compared to those secondary and above level of education (OR = 2.04 95% CI: (1.18, 3.54) and (OR = 2.17 95% CI: 1.12, 4.22), respectively. Conclusion Education appears to be a significant independent factor to determine one’s economic achievement in the studied famine cohort. This may imply, the possible impact of early life famine exposure on economic achievement later in adult life could be modified through better education. Our findings justify the need of expanding education in hunger spots in general and in famine settings in particular.